, 2001). Later studies using irradiation in rodents and more recently using genetically modified mice to inducibly eliminate adult neurogenesis have provided substantial evidence that newborn neurons in the adult brain are required for some, but not all, hippocampus or olfactory bulb-dependent tasks (reviewed by Deng et al., 2010 and Lazarini and Lledo, 2011).
Because of differences in many parameters, such as the timing, duration and cell types of ablation, paradigms of training and behavioral tests, and animals used (age, sex, and genetic background), it is not surprising to find apparent discrepancies in the literature. Collectively, these studies have suggested significant contribution of adult hippocampal
neurogenesis to spatial-navigation learning MI-773 mouse and long-term spatial memory retention, spatial pattern discrimination, trace conditioning and contextual fear conditioning, clearance of hippocampal memory traces, and reorganization of memory to extrahippocampal substrates (reviewed by Deng et al., 2010 and Aimone et al., 2011 in this issue). Adult hippocampal neurogenesis has also been suggested MLN8237 molecular weight to be required for certain, but not all, antidepressant-induced behavioral responses in specific strains of mice (reviewed by Sahay and Hen, 2007 and Sahay et al., 2011 in this issue). The potential role of adult hippocampal neurogenesis in affective behaviors is still under debate. Cumulative evidence has implicated adult olfactory bulb neurogenesis in maintaining long-term structural SB-3CT integrity of the olfactory bulb, short-term olfactory memory, olfactory fear conditioning, and long-term associative olfactory memory involving active learning (reviewed by Lazarini and Lledo, 2011). In addition, olfactory bulb neurogenesis may regulate pheromone-related behaviors, such as mating and social recognition (Feierstein et al., 2010). On
the other hand, aberrant adult neurogenesis contributes to pathophysiological states. For example, seizure-induced SGZ neurogenesis may contribute to epileptogenesis and long-term cognitive impairment (Jessberger et al., 2007 and Kron et al., 2010). One fundamental question is how a small number of newborn neurons can affect global brain function. The answer may reside in the capacity of adult-born neurons both as encoding units and as active modifiers of mature neuron firing, synchronization, and network oscillations (Figure 4). First, adult-born neurons are preferentially activated by specific inputs as indicated by immediate early gene expression in both hippocampus (Kee et al., 2007 and Ramirez-Amaya et al., 2006) and olfactory bulb (Belnoue et al., 2011).
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